Predicting embolic potential during carotid angioplasty and stenting: analysis of captured particulate debris, ultrasound characteristics, and prior carotid endarterectomy.

ABSTRACT

INTRODUCTION: Extracranial carotid stenoses exhibit significant variance in embolic potential, with restenotic lesions having a particularly low propensity for embolization. This study sought to identify characteristics associated with increased generation of embolic debris during carotid angioplasty and stenting (CAS). METHODS: Captured particulate was available for analysis in 56 consecutive patients. Demographics were mean age, 74 years (range, 60-94 years); mean stenosis, 88% (range, 70%-99%); symptomatic, 27%; prior carotid endarterectomy (CEA), 27%; prior radiotherapy, 7%. Plaque echogenicity, heterogenicity, ulceration, and irregularity were assessed with B-mode duplex ultrasound analysis. Gray scale median (GSM) was calculated from normalized B-mode VHS video recordings. Calcification and degree of stenosis were determined angiographically. Captured particulate debris was evaluated for total number; number >200 microm, >500 microm, >1000 microm; mean and median size. Hematoxylin and eosin, trichrome, and von Kossa stains were used for histologic analysis of captured material. RESULTS: Restenotic carotid stenoses after prior CEA generated minimal embolic debris compared with primary stenoses. Four of 15 patients (27%) with restenotic lesions demonstrated embolic particles; all debris was <500 microm. All 41 patients with primary stenoses had some embolic debris; particulate size was >200 microm in 91%, >500 microm in 72%, and >1000 microm in 43%. In primary lesions, the number and size of captured particulate correlated with GSM and with the combined ultrasound findings of echogenicity, heterogenicity, and luminal irregularity/ulceration (P < .02, 95% confidence interval, 4.5-27.6). None of these ultrasound factors correlated independently with embolic particulate (P = NS). Patients aged >70 years exhibited more total particles (8.1 vs 2.3, P = .008) and increased mean particle size (370 vs 157 mum, P = .02). No significant correlation was observed between the number and size of captured embolic particulate and any other variable (stenosis percentage, prior radiotherapy, preprocedural symptoms, periprocedural symptoms, and calcification). Histologically, the embolic debris consisted of extensive amorphous, acellular proteinaceous material. Calcium debris in the embolic particulate was associated with heavily and moderately calcified lesions. CONCLUSIONS: Considerable variation exists in the number and size of embolic particles generated during CAS. Embolic potential is positively correlated with lesion GSM and the combination of lesion echogenicity, heterogenicity, and irregularity. Restenosis after prior CEA is associated with minimal embolic particulate generation, suggesting that embolic protection may not be necessary for CAS of restenotic lesions.